Salidroside alleviates cigarette smoke-induced COPD in mice.

The present study was to evaluate the effects of salidroside (Sal) on CS (cigarette smoke)-induced COPD in mice and explore its underlying mechanisms. 50 male ICR mice were randomly assigned to five groups: control group, CS group, CS+dexamethasone (2mg/kg) group, CS+salidroside (20mg/kg) group and CS+salidroside (40mg/kg) group. The COPD mice were induced by CS exposure for 8 weeks. The results of H&E staining demonstrated that Sal alleviated CS-induced pathological injury in lungs. Besides, Sal increased the activities of superoxide dismutase (SOD), reduced the content of malondialdehyde (MDA) in serum. Sal also inhibited the generations of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in serum and lungs. Furthermore, the administration of Sal significantly inhibited the protein levels of MAPK/NF-κB pathway in CS-induced mice. Our findings showed that Sal might effectively ameliorate the progression of COPD via MAPK/NF-κB pathway.